Shock

Shock is a life-threatening circulatory disorder that leads to tissue hypoxia and a disturbance in microcirculation. There are many different causes of shock, which are classified into hypovolemic shock (e.g., following massive blood/fluid loss), cardiogenic shock (e.g., as a result of acute heart failure), obstructive shock (e.g., due to cardiac tamponade), and distributive shock (due to redistribution of body fluids), which is further classified into septic, anaphylactic, and neurogenic shock. The common clinical findings are hypotension and abnormal heart frequency (most commonly tachycardia; bradycardia in the case of neurogenic shock) accompanied by specific symptoms related to the cause of shock. Diagnosis is mostly made clinical but measurement of functional parameters (e.g., PCWP, CO, SVR) can help distinguish between the different types of shock. Management of shock involves circulatory support and the treatment of the underlying cause. Shock is associated with a very high mortality rate.

General

• Shock: a life-threatening disorder of the circulatory system that results in inadequate organ perfusion and tissue hypoxia, which, in turn, causes metabolic disturbances and, ultimately, irreversible organ damage. ^[1][2]
• Shock index = pulse rate/systolic blood pressure
  • > 1 (positive shock index): indicates shock
  • Normal range: 0.4–0.7

Types of shock

All types of shock, are characterized by low CO and increased SVR, except for septic and anaphylactic shock, which are characterized by high CO and decreased SVR.

General diagnostics

• Assess heart rate, blood pressure, oxygen saturation (pulse oximetry)
• Measure central venous pressure via central venous catheter
• Catheterize the bladder to assess urine output.
• Renal function tests: ↑ BUN and creatinine indicate acute renal failure
• Arterial blood gas analysis: lactic acidosis (commonly elevated in septic shock)
• Clotting parameters: ↓ AT-III, ↓ fibrinogen, and thrombocytopenia, with ↑ fibrin degradation products (FDP) (e.g., D-dimer) indicate a consumption coagulopathy
• Liver function tests: hyperbilirubinemia, ↑ AST/ALT indicate acute liver failure
• Electrolytes (especially sodium, potassium, and calcium)
• See specific diagnostics in respective sections below

General treatment

• Monitor blood pressure and heart rate
• Establish airway, breathing, and circulation (apply high-flow oxygen if necessary)
• See specific treatment in respective sections below

Stages of shock

1. Preshock (nonprogressive phase, stage of compensation): activation of compensatory neurohumoral reflexes in order to maintain vital organ perfusion
   • Peripheral vasoconstriction
     • Manifests with cold, clammy extremities and increased capillary refill time
     • Decreased capillary hydrostatic pressure → increases absorption of interstitial fluids into intravascular space to help maintain blood pressure
     • Peripheral vasoconstriction may be absent in the case of distributive shock.
   • Tachycardia (patients with neurogenic shock may present with bradycardia)
   • Oliguria
2. Shock (progressive phase)
   • Worsening hypotension
   • Hypoperfusion of peripheral tissues → generalized tissue hypoxia → anaerobic metabolism in the underperfused organs → lactic acidosis which in turn causes:
     • Worsening tachypnea
     • Precapillary dilation and postcapillary constriction of the blood vessels → pooling and stasis of blood in the capillary bed → decreased cardiac output and formation of microthrombi in the capillaries → DIC and further hypoxic injury to tissues
   • Acidosis, cerebral hypoperfusion → altered mental status
3. End organ dysfunction (irreversible phase, stage of decompensation): irreversible tissue damage sets in
   • Cerebral hypoxia → autonomic dysfunction
   • Myocardial ischemia → acute coronary syndrome → decreased cardiac output
   • Widespread cell necrosis causes:
     • Release of lysosomal enzymes → further tissue injury → worsening of shock
     • Activation of the immune system → release of cytokines → DIC, further tissue damage
   • Bowel ischemia → bacteremic sepsis
   • The end result of these vicious cycles is a worsening of shock from which there is no recovery (multiple organ failure)

These separate stages may not occur in the case of severe insults (e.g., severe hemorrhage from an abdominal aneurysm, cardiac tamponade). These stages may also not be very distinct in the case of septic shock.

Hypotension, oliguria, tachycardia, and altered mental status indicate that the patient is in shock!

• Etiology
  • Hemorrhage
    • Blunt/penetrating trauma (e.g., pelvic ring/femur fractures)
    • Upper GI bleeding (e.g., variceal bleeding)
    • Postpartum hemorrhage
    • Ruptured aneurysm or hematoma
    • Arteriovenous fistula
  • Nonhemorrhagic fluid loss
    • GI loss: diarrhea, vomiting
    • Increased insensible fluid loss (e.g., burns, Stevens-Johnson syndrome)
    • Third space fluid loss (e.g., bowel obstruction)
    • Renal fluid loss (e.g., adrenal insufficiency, drug-induced diuresis)
• Pathophysiology: loss of intravascular fluid volume → ↓ CO and PCWP → compensatory ↑ SVR
• Clinical features
  • Weak pulse, tachycardia, tachypnea
  • Hypotension
  • Physical examination might show:
    • Cold, clammy extremities, slow capillary refill
    • Decreased skin turgor, dry mucous membranes
    • Nondistended jugular veins
    • Findings related to the underlying disease: e.g., bleeding, melena, hematemesis, diarrhea

• Diagnostics: mostly clinical
  • Imaging to identify the underlying cause such as:
    • X-ray: pelvic ring fractures, hematothorax
    • FAST scan: intra-abdominal hemorrhage
  • ↓ Hemoglobin and hematocrit (can be normal initially )
  • Pulmonary artery catheterization
    • ↓ PCWP (< 15 mmHg)
    • ↓ CO
    • ↑ SVR
• Treatment
  • Fluid resuscitation
  • In the case of hemorrhage
    • Hemostasis
    • Possibly blood transfusion in a 3:1 (fluid-to-blood) ratio ^[3]
• Complications: acute renal failure

Upon suspecting hemorrhage, perform blood grouping and cross-matching and have packed RBC concentrates at hand for transfusion.

• Etiology
  • Myocardial infarction (MI) is the most common cause.
  • Arrhythmias
  • Heart failure
  • Cardiomyopathy
  • Myocarditis
  • Ventricular septal defect, ventricular rupture
  • Severe aortic or mitral regurgitation
  • Certain drugs (e.g., beta blockers, calcium channel blockers)
  • Blunt cardiac trauma
• Pathophysiology: underlying event causes dysfunction of the heart → heart failure → ↓ CO and blood pressure → ↑ catecholamines → vasoconstriction and ↑ myocardial oxygen demand → ↑ renin-angiotensin-aldosterone system → further ↑ vasoconstriction and retention of sodium and water → shunting of blood to brain and vital organs → insufficient perfusion of peripheral organs
• Clinical features
  • Weak pulse, tachycardia
  • Hypotension
  • Dyspnea
  • Mental status change
  • Other clinical features related to the underlying disease:
    • Chest pain in MI
    • Palpitations, syncope in arrhythmias
  • Physical examination might show:
    • Cold, clammy extremities, poor capillary refill
    • Abnormal auscultatory findings (e.g., S₃, S₄)
    • Pulmonary edema, diffuse lung crackles; (fine basal crepitations )
    • Elevated JVP and distended neck veins
• Diagnostics: mostly clinical
  • Identifying the cause
    • ECG: myocardial infarction, cardiac arrhythmias
    • Cardiac markers (e.g., ↑ troponin I, troponin T): to identify acute coronary syndrome
    • Echocardiography: valvular lesions
  • Pulmonary artery catheterization: to monitor hemodynamic parameters as a guide to therapy
    • ↑ PCWP (> 15 mmHg), can also be ↓
    • ↓ CO
    • ↑ SVR
• Treatment: based on the underlying cause
  • Cardiopulmonary resuscitation if necessary
  • Fluid bolus only in cases of decreased blood pressure and/or PCWP < 15 mmHg
  • Inotropic therapy: to maintain perfusion
    • Dopamine in patients with low blood pressure
    • Dobutamine in patients with normal blood pressure
  • Vasopressors: norepinephrine
  • Intra-aortic balloon pump if medical therapy fails
  • Diuresis
  • Treat the underlying cause (e.g., revascularization in MI): See respective treatment sections in the articles listed in “Etiology” above.
  • See “Initial treatment of hemodynamically unstable patients with acute heart failure.”
• Complications
  • Pulmonary edema
  • Acute renal failure

Unlike in other types of shock, the administration of intravenous fluids in most cases of cardiogenic shock worsens cardiogenic pulmonary edema!

• Etiology
  • Impairment of diastolic filling of the right ventricle
    • Cardiac tamponade
    • Constrictive pericarditis
    • Restrictive cardiomyopathy
  • Obstruction of venous return
    • Tension pneumothorax
    • Intrathoracic tumor
  • ↑ Ventricular afterload
    • Massive pulmonary embolism (PE)
    • Aortic dissection
    • Aortic stenosis
    • Large systemic emboli
    • Severe pulmonary hypertension
• Pathophysiology: obstruction of the heart or its great vessels → inability of the heart to circulate blood → ↓ CO → compensatory ↑ SVR
• Clinical features: similar to hypovolemic shock
  • Weak pulse, tachycardia
  • Hypotension
  • Other clinical features related to the underlying disease: chest pain in PE
  • Physical examination might show:
    • Cold, clammy extremities
    • Poor capillary refill
    • Elevated JVP and distended neck veins
• Diagnostics: mostly clinical
  • Identifying the cause
    • Echocardiography: cardiac tamponade
    • CT pulmonary angiography: pulmonary embolism
    • Chest x-ray: pneumothorax
  • Pulmonary artery catheterization: to monitor hemodynamic parameters as a guide to therapy
    • ↓ PCWP, except for cardiac tamponade
      • ↑ PCWP in cardiac tamponade
      • Elevation and equalization of pressures in all the cardiac chambers differentiates cardiac tamponade from other causes of cardiogenic shock.
    • Normal or ↓ CO
    • ↑ SVR
• Treatment: based on the underlying cause
  • Cardiac tamponade: pericardiocentesis
  • Pulmonary embolus: thrombolysis
  • Tension pneumothorax: needle decompression followed by chest tube insertion
• Complications: acute renal failure

• Pathophysiology: redistribution of body fluid due to vasodilation with/without capillary leakage → redistribution of fluid from the intravascular to the extravascular compartment
• Types of distributive shock
  • Septic shock (most common)
  • Neurogenic shock
  • Anaphylactic shock

• Etiology
  • Infection (especially gram-negative bacteria) and bacteremia
  • See “Etiology” in “Sepsis.”
• Pathophysiology: dysregulated host response to infection → capillary leakage, systemic vasodilation → acute and life-threatening organ dysfunction
• Clinical features
  • Fever is typical, but patients may be normothermic or hypothermic
  • Tachycardia
  • Hypotension with a wide pulse pressure
  • Other clinical features related to the underlying disease: cough in pneumonia, neck stiffness in meningitis
  • Physical examination might show:
    • Initially flushed, warm skin (later: cold, pale skin)
    • Normal capillary refill initially
    • Prolonged capillary refill when shock progresses
• Diagnostics: mostly clinical
  • See “Diagnostics” in “Sepsis.”
  • Leukocytosis or leukocytopenia
  • ↑ ESR and acute phase reactants (e.g., CRP, procalcitonin)
  • ↑ Lactate
  • Positive blood cultures
  • Pulmonary artery catheterization
    • ↓ PCWP (< 15 mmHg)
    • ↑ CO
    • ↓ SVR
• Treatment
  • Fluid resuscitation (required until CVP > 8)
  • Vasopressors: in patients refractory to fluids
    • First-line: norepinephrine
    • Second-line: epinephrine
  • Treat the underlying cause
    • Early initiation of broad-spectrum empirical antibiotic therapy (blood cultures should be taken before initiating antibiotic therapy)
    • See “Treatment” in “Sepsis.”
  • Surgical therapy may be required in some cases (e.g., peritonitis, necrotizing fasciitis)
• Complications: acute renal failure

• Etiology
  • Drug reactions (e.g., sulfa drugs)
  • Insect stings or bites (e.g., bee stings)
  • Food allergies (e.g., peanuts)
  • Contrast medium allergy
• Pathophysiology: immunologic anaphylaxis (type I hypersensitivity reaction; IgE-mediated) or nonimmunologic anaphylaxis (not IgE-mediated) → degranulation of mast cells → massive histamine release → systemic vasodilation and increased capillary leakage
• Clinical features: rapid onset of symptoms (minutes to hours)
  • Tachycardia, tachypnea
  • Hypotension
  • Flushed, itchy skin (often hives)
  • Bronchospasm, laryngeal edema → wheeze, stridor, dyspnea, cyanosis
  • Swelling of conjunctiva, lips, tongue and/or uvula
  • Angioedema
  • Vomiting, diarrhea
  • See “Anaphylaxis.”
• Diagnostics: mostly clinical
  • Pulmonary artery catheterization
    • ↓ PCWP (< 15 mmHg)
    • ↑ CO
    • ↓ SVR
• Treatment ^[4]
  • See “Treatment of anaphylaxis.”
  • Fluid resuscitation
  • Epinephrine (1:1000 IM)
  • Adjunctive therapy to epinephrine
    • H1/H2 antihistamines
    • Glucocorticoids (e.g., hydrocortisone)
• Complications
  • Airway obstruction
  • Cardiovascular collapse

• Etiology
  • Spinal cord injury
  • Traumatic brain injury
  • Cerebral hemorrhage
  • Neuraxial anesthesia
• Pathophysiology: damage of autonomic pathways → loss of sympathetic vascular tone → unopposed vagal tone → peripheral vasodilation → pooling of peripheral blood
• Clinical features
  • Bradycardia
  • Hypotension
  • Flushed, warm skin
  • Other clinical features related to the underlying disease: neurological deficits (e.g., flaccid paralysis in spinal trauma)
• Diagnostics
  • Identifying the cause (e.g., imaging for cerebral hemorrhage)
  • Pulmonary artery catheterization
    • ↓ PCWP (< 15 mmHg)
    • ↓ CO
    • ↓ SVR
• Treatment ^[5]
  • Fluid resuscitation
  • Atropine or pacing to treat bradycardia
  • Vasopressors: if fluid resuscitation fails to increase MAP beyond 90 mmHg
    • Normal heart rate: phenylephrine
    • If heart rate < 60/min: epinephrine

In a patient who develops low blood pressure following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive shock have been ruled out.

• One-Minute Telegram 8-2020-2/3: Should a cocktail of vitamin C, thiamine, and hydrocortisone be given to all patients with septic shock?

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1. Kaur P, Basu S, Kaur G, Kaur R. Transfusion protocol in trauma. J Emerg Trauma Shock. 2011; 4 (1): p.103. doi: 10.4103/0974-2700.76844 . | Open in Read by QxMD
2. Campbell RL, Li JTC, Nicklas RA, Sadosty AT. Emergency department diagnosis and treatment of anaphylaxis: a practice parameter. Ann Allergy Asthma Immunol. 2014; 113 (6): p.599-608. doi: 10.1016/j.anai.2014.10.007 . | Open in Read by QxMD
3. Consortium for Spinal Cord Medicine.. Early acute management in adults with spinal cord injury: A clinical practice guideline for health-care professionals.. J Spinal Cord Med. 2008; 31 (4): p.403-79.
4. Hemorrhagic Shock. http://www.cvphysiology.com/Blood%20Pressure/BP031. Updated: April 28, 2014. Accessed: May 31, 2018.
5. Drucker WR, Chadwick CD, Gann DS. Transcapillary refill in hemorrhage and shock.. Arch Surg. 1981; 116 (10): p.1344-53.